Eble JN, Sauter G., Epstein JI, Sesterhenn IA - iarc

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have occasional p63 immunoreactive cells, most representing entrapped benign glands or intraductal spread of carcinoma with residual basal cells {1286}. A Fig. 3.22 A Prostate specific antigen (PSA) expression in prostatic adenocarcinoma with accentuation of glandular luminal spaces. B Metastatic adenocarcinoma to a supraclavicular lymph node labeled staining positively for prostate specific antigen. adenocarcinoma, would be unusual for transitional cell carcinoma {849}. p63 p63, a nuclear protein encoded by a gene on chromosome 3q27-29 with homology to p53 (a tumour suppressor gene), has been shown to regulate growth and development in epithelium of the skin, cervix, breast and urogenital tract. Specific isotypes are expressed in basal cells of pseudostratified epithelia (prostate, bronchial), reserve cells of simple columnar epithelia (endocervical, pancreatic ductal), myoepithelial cells (breast, salivary glands, cutaneous apocrine/eccrine glands), urothelium and squamous epithelium {1286}. A A C monoclonal antibody is active in paraffinembedded tissue following antigen retrieval. p63 has similar applications to those of high molecular weight cytokeratins in the diagnosis of prostatic adenocarcinoma, but with the advantages that p63: 1) stains a subset of 34βE12 negative basal cells, 2) is less susceptible to the staining variability of 34βE12 (particularly in TURP specimens with cautery artefact), and 3) is easier to interpret because of its strong nuclear staining intensity and low background. Interpretative limitations related to presence or absence of basal cells in small numbers of glands for 34βE12 apply to p63, requiring correlation with morphology {2374}. Prostatic adenocarcinomas Fig. 3.23 A H & E stain of adenocarcinoma of the prostate. B Negative staining for high molecular weight cytokeratin in prostate cancer. Note cytoplasmic labeling of basal cells in adjacent benign glands. C Negative staining for p63 in prostate cancer. Note nuclear labeling of basal cells in adjacent benign glands D Positive staining for racemase in adenocarcinoma of the prostate. B B D α-Methyl-CoA racemase (AMACR) AMACR mRNA was recently identified as being overexpressed in prostatic adenocarcinoma by cDNA library subtraction utilizing high throughput RNA microarray analysis {2856}. This mRNA was found to encode a racemase protein, for which polyclonal and monoclonal antibodies have been produced which are active in formalin-fixed, paraffinembedded tissue {187,1220,2856,2935}. Immunohistochemical studies on biopsy material with an antibody directed against AMACR (P504S) demonstrate that over 80% of prostatic adenocarcinomas are labeled {1221,1593}. Certain subtypes of prostate cancer, such as foamy gland carcinoma, atrophic carcinoma, pseudohyperplastic, and treated carcinoma show lower AMACR expression {2936}. However, AMACR is not specific for prostate cancer and is present in nodular hyperplasia (12%), atrophic glands, high grade PIN (>90%) {2935}, and adenosis (atypical adenomatous hyperplasia) (17.5%) {2869}. AMACR may be used as a confirmatory stain for prostatic adenocarcinoma, in conjunction with H&E morphology and a basal cell specific marker {2935}. AMACR is expressed in other non-prostatic neoplasms including urothelial and colon cancer. Androgen receptor (AR) AR is a nuclear localized, androgen binding protein complex occurring in prostatic glandular, basal, stromal cells. The activated protein serves as a transcription factor, mediating androgen dependent cellular functions, e.g. PSA transcription in secretory cells and promoting cellular proliferation. AR monoclonal and polyclonal antibodies are active in formalin-fixed, paraffin-embedded tissue following antigen retrieval {1592,2559}. Positive nuclear staining indicates immunoreactive protein, but does not distinguish active from inactive forms of the protein. AR immunoreactivity was demonstrated in a minority (42.5%) cases of high grade prostatic intraepithelial neoplasia. Most invasive prostatic adenocarcinomas are immunoreactive for AR; one study demonstrated that 85% of untreated 174 Tumours of the prostate
prostate adenocarcinomas exhibit AR immunoreactivity in greater than 50% of tumour cells, with increasing heterogeneity occurring with increasing histologic grade and pathologic stage {1592}. Some studies have shown AR heterogeneity or loss in a subset of AR independent tumours, suggesting one mechanism of androgen resistance may be AR loss {1592,2559}. Because androgen insensitivity may occur without loss of AR immunoreactivity, positive AR immunophenotype may not reliably distinguish androgen dependent from independent tumours {1592}. Imumunostaining for AR is not in routine clinical use. Histologic variants The following histologic variants of prostate adenocarcinoma are typically seen in association with ordinary acinar adenocarcinoma. However, on limited biopsy material, the entire sampled tumour may demonstrate only the variant morphology. Atrophic variant As described under histopathology, most prostate cancers have abundant cytoplasm. An unusual variant of prostate cancer resembles benign atrophy owing to its scant cytoplasm. Although ordinary prostate cancers may develop atrophic cytoplasm as a result of treatment (see carcinoma affected by hormone therapy), atrophic prostate cancers are usually unassociated with such a prior history {467,664}. The diagnosis of carcinoma in these cases may be based on several features. First, atrophic prostate cancer may demonstrate a truly infiltrative process with individual small atrophic glands situated between larger benign glands. In contrast, benign atrophy has a lobular configuration. A characteristic finding in some benign cases of atrophy is the presence of a centrally dilated atrophic gland surrounding by clustered smaller glands, which has been termed "post-atrophic hyperplasia (PAH)" {83}. Although the glands of benign atrophy may appear infiltrative on needle biopsy, they are not truly infiltrative, as individual benign atrophic glands are not seen infiltrating in between larger benign glands. Whereas some forms of atrophy, are associated with fibrosis, atrophic prostate cancer lack such a desmoplastic stromal response. Atrophic prostate cancer may also be differentiated from benign atrophy by the presence of marked cytologic atypia. Atrophy may show enlarged nuclei and prominent nucleoli, although not the huge eosinophilic nucleoli seen in some atrophic prostate cancers. Finally, the concomitant presence of ordinary less atrophic carcinoma can help in recognizing the malignant nature of the adjacent atrophic cancer glands. Pseudohyperplastic variant Pseudohyperplastic prostate cancer resembles benign prostate glands in that the neoplastic glands are large with branching and papillary infolding {1146, 1485}. The recognition of cancer with this pattern is based on the architectural pattern of numerous closely packed glands as well as nuclear features more typical of carcinoma. One pattern of pseudohyperplastic adenocarcinoma consists of numerous large glands that are almost back-to-back with straight even luminal borders, and abundant cytoplasm. Comparably sized benign glands either have papillary infoldings or are atrophic. The presence of cytologic atypia in some of these glands further distinguishes them from benign glands. It is almost always helpful to verify pseudohyperplastic cancer with the use of immunohistochemistry to verify the absence of basal cells. Pseudohyperplastic cancer, despite its benign appearance, may be associated with typical intermediate grade cancer and can exhibit aggressive behaviour (ie., extraprostatic extension). Foamy gland variant Foamy gland cancer is a variant of acinar adenocarcinoma of the prostate that is characterized by having abundant foamy appearing cytoplasm with a very low nuclear to cytoplasmic ratio. Although the cytoplasm has a xanthomatous appearance, it does not contain lipid, but rather empty vacuoles {2637}. More typical cytological features of adenocarcinoma such as nuclear enlargement and prominent nucleoli are frequently absent, which makes this lesion difficult to recognize as carcinoma especially on biopsy material. Characteristically, the nuclei in foamy gland carcinoma are small and densely hyperchromatic. Nuclei in foamy gland cancer are round, more so than those of benign prostatic secretory cells. In addition to the unique nature of its cytoplasm, it is recognized as carcinoma by its architectural pattern of crowded and/or infiltrative glands, and frequently present dense pink acellular secretions {1880}. In most cases, foamy gland cancer is seen in association with ordinary A B Fig. 3.24 Atrophic adenocarcinoma. A Note the microcystic pattern and B the prominent nucleoli. Acinar adenocarcinoma 175
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World Health Organization Classific
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This volume was produced in collabo
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Contents 1 Tumours of the kidney 9
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CHAPTER 1 Tumours of the Kidney Can
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TNM classification of renal cell ca
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one quarter of kidney cancers in bo
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Familial renal cell carcinoma M.J.
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Table 1.02 Genotype - phenotype cor
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A B Fig. 1.11 A Multiple cutaneous
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A B Fig. 1.14 Birt-Hogg-Dubé syndr
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Clear cell renal cell carcinoma D.J
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Fig. 1.20 Clear cell renal cell car
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Papillary renal cell carcinoma B. D
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A B Fig. 1.29 Papillary renal cell
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Fig. 1.33 Chromophobe RCC with sarc
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Carcinoma of the collecting ducts o
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Renal medullary carcinoma C.J. Davi
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Renal carcinomas associated with Xp
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Renal cell carcinoma associated wit
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Papillary adenoma of the kidney J.N
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of this tumour. Microscopic extensi
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A B Fig. 1.59 Metanephric adenoma.
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esults in intratumoral aneurysms. O
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peritumoural fibrous pseudocapsule.
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increases in prevalence to approxim
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Nephrogenic rests and nephroblastom
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Cystic partially differentiated nep
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A B Fig. 1.80 Clear cell sarcoma of
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A B Fig. 1.85 Rhabdoid tumour of th
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transcription factor is fused to th
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Leiomyosarcoma S.M. Bonsib Definiti
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Angiomyolipoma G. Martignoni M.B. A
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melanocytic and smooth muscle marke
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Multinucleated and enlarged ganglio
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Haemangioma P. Tamboli Definition H
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Fig. 1.107 Juxtaglomerular cell tum
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Intrarenal schwannoma I. Alvarado-C
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Mixed epithelial and stromal tumour
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Synovial sarcoma of the kidney J.Y.
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Renal carcinoid tumour L.R. Bégin
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Primitive neuroectodermal tumour (E
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Paraganglioma / Phaeochromocytoma P
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Leukaemia A. Orazi Interstitial inf
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WHO histological classification of
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TNM classification of carcinomas of
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The risk of bladder cancer goes dow
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Tumour spread and staging Urinary b
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feature in such patients undergoing
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A Fig. 2.12 Infiltrative urothelial
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A Fig. 2.15 A Infiltrating urotheli
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A B Fig. 2.19 A Infiltrative urothe
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Fig. 2.23 Infiltrative urothelial c
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ing systems have been proposed on t
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Non-invasive urothelial tumours G.
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chronically inflamed urothelium and
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Inverted papilloma G. Sauter Defini
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muscle invasive disease, but there
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Fig. 2.42 Non-invasive urothelial n
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A Fig. 2.45 Non-invasive urothelial
Page 119 and 120: for DBCCR1 silencing {984,2476}. Th
Page 121 and 122: Squamous cell carcinoma D.J. Grigno
Page 123 and 124: Fig. 2.51 Squamous cell carcinoma.
Page 125 and 126: Adenocarcinoma A.G. Ayala P. Tambol
Page 127 and 128: A B Fig. 2.61 A Adenocarcinoma in s
Page 129 and 130: A B Fig. 2.65 Intramural urachal ca
Page 131 and 132: Müllerian origin is postulated for
Page 133 and 134: A Fig. 2.69 Small cell carcinoma. A
Page 135 and 136: Carcinoid L. Cheng Definition Carci
Page 137 and 138: Leiomyosarcoma J. Cheville Definiti
Page 139 and 140: Osteosarcoma L. Guillou Definition
Page 141 and 142: Leiomyoma J. Cheville Definition A
Page 143 and 144: Haemangioma L. Cheng Definition Hae
Page 145 and 146: Metastatic tumours and secondary ex
Page 147 and 148: Tumours of the renal pelvis and ure
Page 149 and 150: nodular, ulcerative or infiltrative
Page 151 and 152: Tumours of the urethra F. Hofstädt
Page 153 and 154: usually show enteric, colloid or si
Page 155 and 156: CHAPTER 3X Tumours of of the the Pr
Page 157 and 158: TNM classification of carcinomas of
Page 159 and 160: contrast, mortality among migrants
Page 161 and 162: Fig. 3.06 Transrectal ultrasound of
Page 163 and 164: PSA-related diagnostic strategies.
Page 165 and 166: A B C Fig. 3.10 A,B Section of pros
Page 167 and 168: pale-clear, similar to benign gland
Page 169: A B Fig. 3.20 A, B Adenocarcinoma w
Page 173 and 174: A Fig. 3.27 A, B Foamy gland adenoc
Page 175 and 176: A B Fig. 3.32 A Sarcomatoid carcino
Page 177 and 178: A B Fig. 3.37 A Gleason score 1+1=2
Page 179 and 180: A B Fig. 3.43 A Prostate cancer Gle
Page 181 and 182: Fig. 3.48 Heat map-nature. From S.M
Page 183 and 184: Fig. 3.51 Prostate cancer. Major su
Page 185 and 186: many stage T1b cancers. Stage T2 Mo
Page 187 and 188: Fig. 3.58 Patterns of seminal vesic
Page 189 and 190: Prostatic intraepithelial neoplasia
Page 191 and 192: A B Fig. 3.63 A Micropapillary high
Page 193 and 194: A B Fig. 3.68 A Ductal carcinoma in
Page 195 and 196: Ductal adenocarcinoma X.J. Yang L.
Page 197 and 198: Papillary pattern can be seen in bo
Page 199 and 200: A B Fig. 3.74 A Inflammation withou
Page 201 and 202: Squamous neoplasms T.H. Van der Kwa
Page 203 and 204: Neuroendocrine tumours P.A. di Sant
Page 205 and 206: Mesenchymal tumours J. Cheville F.
Page 207 and 208: Fig. 3.89 Sarcoma of the prostate.
Page 209 and 210: Miscellaneous tumours P.H. Tan L. C
Page 211 and 212: A Fig. 3.96 A Adenocarcinoma of the
Page 213 and 214: WHO histological classification of
Page 215 and 216: Introduction F.K. Mostofi I.A. Sest
Page 217 and 218: wartime birth cohorts illustrate th
Page 219 and 220: Similar tumours as those of group 1
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crucial for the development of this
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A B Fig. 4.09 Spermatocytic seminom
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A B Fig. 4.14 Intratubular germ cel
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A B Fig. 4.19 Seminoma. A Typical s
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Fig. 4.24 Seminoma. Vascular invasi
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Fig. 4.28 Spermatocytic seminoma wi
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A B Fig. 4.33 Embryonal carcinoma.
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A B Fig. 4.38 Yolk sac tumour. A En
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have cytoplasmic lacunae that conta
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A Fig. 4.46 Teratoma. A Longitudina
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A B Fig. 4.51 A Cut surface of derm
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Fig. 4.54 Mixed germ cell tumour. L
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Sex cord / gonadal stromal tumours
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A B C Fig. 4.67 Malignant Leydig ce
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A Fig. 4.73 A Sertoli cell tumour.
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ICD-O codes Granulosa cell tumour 8
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ICD-O code 8592/1 Clinical features
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A B Fig. 4.83 Germ cell-sex cord/go
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A Fig. 4.85 A, B Brenner tumour of
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typical grade III follicular morpho
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testicular parenchyma and tumour te
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A B the surgical scar and adjacent
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Immunoprofile Ordóñez and associa
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often have a grey-white cut surface
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Fig. 4.111 Angiomyofibroblastoma-li
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A B Fig. 4.119 Embryonal rhabdomyos
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Table 4.05 Secondary tumours of the
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WHO histological classification of
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A Fig. 5.04 A, B Squamous cell carc
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deformed by an exophytic mass. In s
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A B C Fig. 5.12 A Warty (condylomat
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A Fig. 5.20 Bowenoid papulosis. A,
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three had been circumcized by 9 yea
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Mesenchymal tumours J.F. Fetsch M.
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Fig. 5.31 Neurofibroma of the penis
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oectodermal tumour/Ewing sarcoma [p
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Secondary tumours of the penis C.J.
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Dr John N. EBLE* Dept. of Pathology
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Dr Ricardo PANIAGUA Department of C
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Source of charts and photographs 1.
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References 1. Anon. (1955). Case re
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115. Ariel I, Sughayer M, Fellig Y,
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246. Birt AR, Hogg GR, Dube WJ (197
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374. Cardone G, Malventi M, Roffi M
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502. Corti B, Carella R, Gabusi E,
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633. Donhuijsen K, Schmidt U, Richt
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768. Fischer J, Palmedo G, von Knob
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900. Goedert JJ, Cote TR, Virgo P,
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1028. Hartmann A, Dietmaier W, Hofs
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1162. Iezzoni JC, Fechner RE, Wong
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1293. Keetch DW, Catalona WJ (1995)
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1424. Ladanyi M, Lui MY, Antonescu
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1548. Lopez-Beltran A, Croghan GA,
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1681. McLaughlin JK, Silverman DT,
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1816. Moudouni SM, En-Nia I, Rioux-
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1945. Ohori M, Wheeler TM, Kattan M
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2070. Phillips G, Kumari-Subaiya S,
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2199. Riou G, Barrois M, Prost S, T
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2327. Schmidt L, Junker K, Weirich
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2450. Smith G, Elton RA, Beynon LL,
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2572. Tamboli P, Mohsin SK, Hailema
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2693. van Echten J, Timmer A, van d
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2816. Wick MR, Berg LC, Hertz MI (1
Page 347 and 348:
2937. Zhuang Z, Park WS, Pack S, Sc
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CCNB, 226 CCND1, 105, 108 CCND2, 22
Page 351 and 352:
J Juvenile type granulosa cell tumo
Page 353 and 354:
Promoter methylation, 21 Prostate s
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